<i>Campylobacter</i>
            gene polymorphism as a determinant of clinical features of Guillain–Barré syndrome

Koga, Michiaki; Takahashi, Masaki; Masuda, Midori; Hirata, Koichi; Yuki, Nobuhiro

doi:10.1212/01.wnl.0000176914.70893.14

Cited by 105 publications

(61 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…C jejuni (CstII [Asn51]) strains produce GD1c- or GT1a-like lipo-oligosaccharide (figure 2). 54 Patients who are infected with these C jejuni strains go on to produce IgG anti-GQ1b antibodies in patients with certain immunogenetic backgrounds. As previously discussed, binding of the anti-GQ1b antibodies to the oculomotor, trochlear and abducens nerves as well as muscle spindles in the limbs21 43 results in the ophthalmoplegia and ataxia that is observed in the anti-GQ1b antibody syndrome.…”

Section: Pathophysiologymentioning

confidence: 99%

“…The 51st amino acid of CstII determines its enzymatic activity: CstII (Thr51) produces GM1- and GD1a-like lipo-oligosaccharides, whereas Cst-II (Asn51) synthesises lipo-oligosaccharides mimicking GQ1b 52 . C jejuni isolates that have cst-II (Asn51) bear lipo-oligosaccharides mimicking GQ1b, and infection by such strains may elicit the generation of immunoglobulin G (IgG) anti-GQ1b antibodies 54. The autoantibodies upon binding to GQ1b expressed in the oculomotor, trochlear and abducens nerves as well as in the muscle spindles in the limbs would cause FS 21 43.…”

Section: Pathophysiologymentioning

confidence: 99%

“…In support of this, an FS isolate has been shown to carry GT1a-like lipo-oligosaccharides as well as GM1- and GD1a-like lipo-oligosaccharides as shown in the biosynthesis pathway (figure 2). 54 Therefore, depending on the infective strains harboured by the susceptible patient, any clinical phenotype can be present throughout the illness and can range from the milder spectrum of incomplete FS to either FS or BBE to the more extensive cases where there is an overlap with PCB or GBS.…”

Section: Pathophysiologymentioning

confidence: 99%

See 2 more Smart Citations

Bickerstaff brainstem encephalitis and Fisher syndrome: anti-GQ1b antibody syndrome

Shahrizaila

Yuki

2012

Journal of Neurology, Neurosurgery & Psychiatry

Self Cite

240

184

View full text Add to dashboard Cite

Section: Pathophysiologymentioning

confidence: 99%

Section: Pathophysiologymentioning

confidence: 99%

Section: Pathophysiologymentioning

confidence: 99%

See 1 more Smart Citation

Bickerstaff brainstem encephalitis and Fisher syndrome: anti-GQ1b antibody syndrome

Shahrizaila

Yuki

2012

Journal of Neurology, Neurosurgery & Psychiatry

Self Cite

240

184

View full text Add to dashboard Cite

“…Molecular mimicry has been well-described between GM1 and GD1a gangliosides and lipo-oligosaccharide components of C. jejuni , the commonest identified antecedent infection in AMAN,13 while other strains of C. jejuni with disialylated lipo-oligosachharides induce the GQ1b ganglioside antibodies associated with Miller-Fisher syndrome (MFS) 14. However, the pathogenic mechanisms in acute inflammatory demyelinating polyneuropathy (AIDP) are less clear with both cellular15 16 and humoral immune responses reported 17 18.…”

Section: Introductionmentioning

confidence: 99%

Seasonal variation in Guillain-Barré syndrome: a systematic review, meta-analysis and Oxfordshire cohort study

Webb

Brain

Wood

et al. 2014

J Neurol Neurosurg Psychiatry

View full text Add to dashboard Cite

Introduction Evidence for seasonal variation in incidence and subtype of Guillain-Barré syndrome (GBS) is contradictory, but has implications for provision of neurological services and understanding pathogenesis. Methods We searched PubMed and EMBASE between inception and January 2014, including all studies reporting seasonal incidence of GBS. We included a retrospective cohort study of patients with GBS at the John Radcliffe Hospital, Oxford 2001-2012 and determined the seasonal variation in GBS incidence and length of stay. The incidence rate ratio (IRR) for winter versus summer was pooled across studies by fixed and random effects meta-analysis weighted by inverse variance, stratified by geographical region, infectious prodrome and GBS subtype.

show abstract

“…In addition, bacterial Sias can enhance intracellular survival (5), participate in biofilm formation (6), or mask underlying antibody epitopes (7). Antibodies elicited against sialylated bacterial glycolipids can also cross-react with host peripheral nerve axons, leading to the debilitating autoimmune disorder called GuillainBarré syndrome (8,9). In short, there are multiple Sia-dependent virulence mechanisms that enhance bacterial survival and/or result in host tissue injury.…”

mentioning

confidence: 99%

The Group B Streptococcal Sialic Acid O-Acetyltransferase Is Encoded by neuD, a Conserved Component of Bacterial Sialic Acid Biosynthetic Gene Clusters

Lewis

Hensler

Varki

et al. 2006

Journal of Biological Chemistry

View full text Add to dashboard Cite

Nearly two dozen microbial pathogens have surface polysaccharides or lipo-oligosaccharides that contain sialic acid (Sia), and several Sia-dependent virulence mechanisms are known to enhance bacterial survival or result in host tissue injury. Some pathogens are also known to O-acetylate their Sias, although the role of this modification in pathogenesis remains unclear. We report that neuD, a gene located within the Group B Streptococcus (GBS) Sia biosynthetic gene cluster, encodes a Sia O-acetyltransferase that is itself required for capsular polysaccharide (CPS) sialylation. Homology modeling and site-directed mutagenesis identified Lys-123 as a critical residue for Sia O-acetyltransferase activity. Moreover, a single nucleotide polymorphism in neuD can determine whether GBS displays a "high" or "low" Sia O-acetylation phenotype. Complementation analysis revealed that Escherichia coli K1 NeuD also functions as a Sia O-acetyltransferase in GBS. In fact, NeuD homologs are commonly found within Sia biosynthetic gene clusters. A bioinformatic approach identified 18 bacterial species with a Sia biosynthetic gene cluster that included neuD. Included in this list are the sialylated human pathogens Legionella pneumophila, Vibrio parahemeolyticus, Pseudomonas aeruginosa, and Campylobacter jejuni, as well as an additional 12 bacterial species never before analyzed for Sia expression. Phylogenetic analysis shows that NeuD homologs of sialylated pathogens share a common evolutionary lineage distinct from the poly-Sia O-acetyltransferase of E. coli K1. These studies define a molecular genetic approach for the selective elimination of GBS Sia O-acetylation without concurrent loss of sialylation, a key to further studies addressing the role(s) of this modification in bacterial virulence.Sialic acids (Sias) 3 are a family of related nine-carbon acidic sugars (nonulosonic acids) that are found at the outer ends of glycan chains on all vertebrate cells. Over 20 microbial pathogens are known to use surface Sia decoration as a form of molecular mimicry that is often crucial to virulence (1). Several convergent strategies for microbial Sia decoration have been identified, including endogenous biosynthesis, scavenging, or direct transfer of host Sias to their own surface glycans (1). Heavily sialylated bacteria often cause sepsis and meningitis by exhibiting Sia-dependent serum resistance due to deactivation of the alternative complement pathway (2-4). In addition, bacterial Sias can enhance intracellular survival (5), participate in biofilm formation (6), or mask underlying antibody epitopes (7). Antibodies elicited against sialylated bacterial glycolipids can also cross-react with host peripheral nerve axons, leading to the debilitating autoimmune disorder called GuillainBarré syndrome (8, 9). In short, there are multiple Sia-dependent virulence mechanisms that enhance bacterial survival and/or result in host tissue injury.Several pathogenic bacteria are known to modify Sia residues by O-acetylation (10 -18). In other contexts, ...

show abstract

Campylobacter gene polymorphism as a determinant of clinical features of Guillain–Barré syndrome

Cited by 105 publications

References 44 publications

Bickerstaff brainstem encephalitis and Fisher syndrome: anti-GQ1b antibody syndrome

Bickerstaff brainstem encephalitis and Fisher syndrome: anti-GQ1b antibody syndrome

Seasonal variation in Guillain-Barré syndrome: a systematic review, meta-analysis and Oxfordshire cohort study

The Group B Streptococcal Sialic Acid O-Acetyltransferase Is Encoded by neuD, a Conserved Component of Bacterial Sialic Acid Biosynthetic Gene Clusters

Contact Info

Product

Resources

About